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- Mishra, A, et al.
(författare)
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Diminishing benefits of urban living for children and adolescents' growth and development
- 2023
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Ingår i: Nature. - : Springer Science and Business Media LLC. - 1476-4687 .- 0028-0836. ; 615:7954, s. 874-883
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Tidskriftsartikel (refereegranskat)abstract
- Optimal growth and development in childhood and adolescence is crucial for lifelong health and well-being1–6. Here we used data from 2,325 population-based studies, with measurements of height and weight from 71 million participants, to report the height and body-mass index (BMI) of children and adolescents aged 5–19 years on the basis of rural and urban place of residence in 200 countries and territories from 1990 to 2020. In 1990, children and adolescents residing in cities were taller than their rural counterparts in all but a few high-income countries. By 2020, the urban height advantage became smaller in most countries, and in many high-income western countries it reversed into a small urban-based disadvantage. The exception was for boys in most countries in sub-Saharan Africa and in some countries in Oceania, south Asia and the region of central Asia, Middle East and north Africa. In these countries, successive cohorts of boys from rural places either did not gain height or possibly became shorter, and hence fell further behind their urban peers. The difference between the age-standardized mean BMI of children in urban and rural areas was <1.1 kg m–2 in the vast majority of countries. Within this small range, BMI increased slightly more in cities than in rural areas, except in south Asia, sub-Saharan Africa and some countries in central and eastern Europe. Our results show that in much of the world, the growth and developmental advantages of living in cities have diminished in the twenty-first century, whereas in much of sub-Saharan Africa they have amplified.
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- Adcox, K, et al.
(författare)
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PHENIX detector overview
- 2003
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Ingår i: Nuclear Instruments & Methods in Physics Research. Section A: Accelerators, Spectrometers, Detectors, and Associated Equipment. - 0167-5087. ; 499:2-3, s. 469-479
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Tidskriftsartikel (refereegranskat)abstract
- The PHENIX detector is designed to perform a broad study of A-A, p-A, and p-p collisions to investigate nuclear matter under extreme conditions. A wide variety of probes, sensitive to all timescales, are used to study systematic variations with species and energy as well as to measure the spin structure of the nucleon. Designing for the needs of the heavy-ion and polarized-proton programs has produced a detector with unparalleled capabilities. PHENIX measures electron and muon pairs, photons, and hadrons with excellent energy and momentum resolution. The detector consists of a large number of subsystems that are discussed in other papers in this volume. The overall design parameters of the detector are presented. (C) 2002 Elsevier Science B.V. All rights reserved.
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- Adler, SS, et al.
(författare)
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PHENIX on-line systems
- 2003
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Ingår i: Nuclear Instruments & Methods in Physics Research. Section A: Accelerators, Spectrometers, Detectors, and Associated Equipment. - 0167-5087. ; 499:2-3, s. 560-592
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Tidskriftsartikel (refereegranskat)abstract
- The PHENIX On-Line system takes signals from the Front End Modules (FEM) on each detector subsystem for the purpose of generating events for physics analysis. Processing of event data begins when the Data Collection Modules (DCM) receive data via fiber-optic links from the FEMs. The DCMs format and zero suppress the data and generate data packets. These packets go to the Event Builders (EvB) that assemble the events in final form. The Level-1 trigger (LVL1) generates a decision for each beam crossing and eliminates uninteresting events. The FEMs carry out all detector processing of the data so that it is delivered to the DCMs using a standard format. The FEMs also provide buffering for LVL1 trigger processing and DCM data collection. This is carried out using an architecture that is pipelined and deadtimeless. All of this is controlled by the Master Timing System (MTS) that distributes the RHIC clocks. A Level-2 trigger (LVL2) gives additional discrimination. A description of the components and operation of the PHENIX On-Line system is given and the solution to a number of electronic infrastructure problems are discussed. (C) 2002 Elsevier Science B.V. All rights reserved.
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- Yao, Q, et al.
(författare)
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Inhibition of the effect of high glucose on the expression of Smad in human peritoneal mesothelial cells
- 2004
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Ingår i: The International journal of artificial organs. - : SAGE Publications. - 0391-3988 .- 1724-6040. ; 27:10, s. 828-834
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Tidskriftsartikel (refereegranskat)abstract
- As high glucose (HG) concentration in peritoneal dialysis (PD) solution is thought to contribute to peritoneal fibrosis, and angiotensin II receptor blockers (ARBs) may have a key role in preventing fibrosis as they may inhibit the TGF- ß1–Smad pathway, the aims of this in vitro study were to investigate 1) if HG affects the expression of Smad in human peritoneal mesothelial cells (HPMCs) and 2) if ARB (losartan) can inhibit this effect. Methods HPMCs, obtained from non-renal patients undergoing elective abdominal surgery, were stimulated by HG solutions with different concentrations (1.5%, 2.5%, 4.25%) of dextrose and mannitol, and by solutions containing combination with dextrose and losartan. The supernatant was assayed for TGF- ß1 by ELISA and cells were collected for the analysis of Smad family by RT-PCR and Western Blot. Results 1) HG up-regulated the expression of Smad2 on both gene and protein levels, especially in 2.5% and 4.25% dextrose groups (P&0.05), and also stimulated the expression of Smad4 in 4.25% dextrose group. However, the expression of Smad3 was not affected. 2) High osmolality as such (using mannitol) did not affect the TGF-ß1-Smad signaling pathway. 3) Losartan inhibited the expression of Smad2 on the gene level but not on the protein level. 4) HG up-regulated the level of TGF- ß1 with increasing dextrose concentration, while losartan partially inhibited this effect of HG on releasing of TGF-ß1. Conclusion A high glucose solution up-regulated the expression of Smad2 and Smad4, suggesting that the TGF- ß1-Smad pathway could be involved in the fibrosis of the peritoneum during PD. As losartan inhibited the expression of Smad2 on the gene level and reduced the concentration of TGF- ß1 in our study, the results of this in vitro study suggest that the use of angiotensin II receptor blockers might represent a possible way to prevent and treat peritoneal fibrosis in PD patients. However, further studies in vivo are needed to confirm this hypothesis.
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